Human C1 inhibitor (C1INH) has been shown to effect human neutrophil chemotaxis in either a positive (enhancement) or a negative (inhibition) fashion depending on the source of cytotaxin. When normal human plasma is used as a source of cytotaxin by generation with zymosan, lipopolysaccharide, and immune complexes, C1INH effects enhancement. When human C3a or C5a or guinea pig C5a is used as cytotaxin, C1INH effects inhibition. The action of C1INH is apparently directly on the neutrophils and functions at physiological concentrations. C1INH has also been shown to enhance the chemotactic response of neutrophils to the dipeptide (DP) N-formylmethionylphenylalanine. C1INH has been found to have an effect on chemotactic deactivation of human neutrophils. When C1INH is present with the neutrophils during deactivation, prevention of this process is found. When C1INH is present with deactivated neutrophils during migration in Boyden chambers, this phenomenon is reversed. Therefore, C1INH will both inhibit and reverse neutrophil deactivation. Human neutrophil deactivation has been established with DP. Heparin has been found to enhance the random migration of human neutrophils which is dependent upon the presence of serum factors. BIBLIOGRAPHIC REFERENCE: Smith, C. W., J. C. Hollers, D. H. Bing and R. A. Patrick. 1975. Effects of human CI inhibitor on complement-mediated human leukocyte chemotaxis. J. Immunol. 114:216.